The central modulatory effect of clonidine on the cardiodepressor reflex after suppression of synthesis and storage of noradrenaline.

Rats were decerebrated and treated with a β-adrenoceptor blocker (toliprolol, Kö 592, 5 mg/kg). Increase of blood pressure were repeatedly elicited by i.v. injection of angiotensin (0.03–0.125 μg/kg) and the accompanying reflex bradycardia was measured. The vagally mediated reflex bradycardia was significantly increased by clonidine, 30 μg/kg i.v., in non-pretreated animals as well as after pretreatment with reserpine (7.5 mg/kg s.c., 20 hr) and α-methyl-p-tyrosine-methylester (250 mg/kg i.p., 5 hr), separately or in combination. The facilitatory effect of clonidine was antagonized in all groups by i.v. injection of the α-adrenoceptor blocking drugs, phentolamine (5 mg/kg) and piperoxan (1 mg/kg). In the control periods before clonidine, reflex bradycardia was similar in pretreated animals to that in animals without pretreatment. It was concluded therefore that catecholamines have no essential transmitter functions in the cardiodepressor reflex loop. Therefore, the action of clonidine on cardiovascular centers in the medulla is independent of endogenous noradrenaline storage and synthesis. A direct effect is assumed on central α-adrenoceptors, which have a modulatory ‘effector’ function on the cardiodepressor reflex.